Evidence mapPaperPMID 41044889Full record

ReviewEuropean journal of clinical investigation2026

Lipoprotein(a) in clinical practice: Risk stratification and therapeutic strategies.

Nadim Nasrallah, Mark Atallah, Tarek Harb, Gary Gerstenblith, Thorsten M Leucker

Abstract readReview
In one paragraph

Review in European journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Nadim NasrallahDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mark AtallahDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tarek HarbDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Gary GerstenblithDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Thorsten M LeuckerDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0003-2569-6617

Funding

Lipoprotein (a) Modification of the Impact of HIV Infection on Atherosclerotic Cardiovascular DiseaseR01HL176322 · JOHNS HOPKINS UNIVERSITY · 2025 to 2025
$713k
NHLBI NIH HHS R01 HL176322
6 · The paper itself

Abstract

backgroundLipoprotein(a) [Lp(a)] is a primarily genetically determined, causal and independent risk factor for atherosclerotic cardiovascular disease (ASCVD). Lp(a) levels are stable, unaffected by lifestyle, and best measured using isoform-insensitive, molar-based assays. Current guidelines from the European Atherosclerosis Society and U.S. National Lipid Association recommend a one-time Lp(a) measurement in all adults. Cascade testing is advised in affected families.

resultsElevated Lp(a) levels are associated with increased risk of coronary artery disease, myocardial infarction incidence and recurrence, and aortic stenosis onset and progression. In cerebrovascular disease, high Lp(a) is linked to large artery ischemic stroke incidence and recurrence, as well as poor functional outcomes. Associations with venous thromboembolism are limited to prothrombotic states and extreme Lp(a) concentrations. Elevated levels (≥50 mg/dL or ≥125 nmol/L) should prompt intensified risk factor modification.

conclusionThere are no currently approved lipid-lowering therapies that substantially reduce Lp(a) levels. Novel agents to lower Lp(a) include antisense oligonucleotides, small interfering ribonucleic acid and small molecules, all of which have shown promising results in phase 2 trials. Ongoing phase 3 trials will evaluate the causal relationship between Lp(a) and ASCVD, and whether lowering Lp(a) reduces cardiovascular outcomes.

Indexed as

AtherosclerosisCardiovascular DiseasesCoronary Artery DiseaseLipoprotein(a)Aortic Valve StenosisCerebrovascular DisordersHumansHypolipidemic AgentsMyocardial InfarctionOligonucleotides, AntisenseRisk AssessmentRisk FactorsVenous ThromboembolismHypolipidemic AgentsLipoprotein(a)Oligonucleotides, Antisenseacute coronary syndromeaortic stenosisASCVDcardiovascular disease preventionlipoprotein(a)risk stratification

Identifiers

PMID41044889
PMCPMC13383082

What Socratic holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.